Nasal Septal Haematoma: A Complication of Nasal Trauma

Nasal septal haematoma is a serious complication that can occur after even minor nasal trauma. It is characterized by the accumulation of blood between the septal cartilage and the surrounding perichondrium. The most common symptom is nasal obstruction, but pain and rhinorrhoea may also be present. On examination, a bilateral, red swelling arising from the nasal septum is typically seen. It is important to differentiate this from a deviated septum, which will be firm to the touch.

If left untreated, nasal septal haematoma can lead to irreversible septal necrosis within just a few days. This occurs due to pressure-related ischaemia of the cartilage, which can result in necrosis and a saddle-nose deformity. To prevent this, surgical drainage and intravenous antibiotics are necessary. It is important to be vigilant for this complication after any nasal trauma, no matter how minor.

Recommendations for a Couple Struggling with Infertility

When a couple is struggling to conceive, there are several recommendations that healthcare providers may suggest. Firstly, if the couple has been trying to conceive for a year without success, they should be referred to fertility services. However, if there is an underlying reason for conception difficulties, earlier investigation may be necessary. In cases where the male partner is taking non-steroidal anti-inflammatory drugs, there is no impact on his ability to conceive. A hernia repair is not indicated to improve the couple’s chances of conception. Watching and waiting is not appropriate, and referral to fertility services is recommended. Finally, while sertraline and other SSRIs are not teratogenic, they can cause sexual dysfunction, which should be explored with the patient.

When a woman expresses interest in starting hormone replacement therapy (HRT), it is important to gather a detailed medical history to determine her menopausal status. This includes information about her last menstrual period (LMP) and any bleeding patterns leading up to it. Based on this information, it appears that the woman in question is peri-menopausal, as she has not been without a period for a full year.

The primary reason for starting HRT is to alleviate vasomotor symptoms, such as hot flashes. However, it may also be used to prevent osteoporosis in women who have been diagnosed with premature menopause.

For women who still have a uterus, HRT should consist of a combination of estrogen and progesterone. The progesterone is essential for reducing the risk of endometrial cancer, which can occur when estrogen is used alone. Women who have had a hysterectomy will typically receive continuous estrogen-only therapy.

The type of HRT prescribed will depend on the woman’s menopausal status. Those who have had their LMP within the past year should receive cyclical combined HRT, while those who have been without a period for at least a year or who have experienced premature menopause should receive continuous combined HRT.

For women who are unable or unwilling to take HRT, there are several non-hormonal treatments available for vasomotor symptoms. These include certain selective serotonin and noradrenaline reuptake inhibitors, clonidine, and gabapentin. However, sertraline is not effective for treating hot flashes. It is worth noting that the National Institute for Health and Clinical Excellence (NICE) does not recommend the use of herbal or complementary therapies for managing hot flashes and night sweats.

Hormone replacement therapy (HRT) involves a small dose of oestrogen and progestogen to alleviate menopausal symptoms. The indications for HRT have changed due to the long-term risks, and it is primarily used for vasomotor symptoms and preventing osteoporosis in younger women. HRT consists of natural oestrogens and synthetic progestogens, and can be taken orally or transdermally. Transdermal is preferred for women at risk of venous thromboembolism.

The use of COCP is absolutely contraindicated for individuals who are over 35 years old and smoke more than 15 cigarettes per day. Migraine without aura is not a contraindication, but migraine with aura is a UKMEC 3 contraindication. A BMI of over 35 kg/m2 and a family history of thromboembolism at age less than 45 years are also UKMEC 3 contraindications, but in this case, the patient’s BMI is 25 kg/m2 and her mother had pulmonary embolism at the age of 60 years, so these are not contraindications. Breastfeeding less than 6 weeks post-partum is a UKMEC 4 contraindication, but since the patient is 10 weeks post-partum, it is a UKMEC 2.

The decision to prescribe the combined oral contraceptive pill is now based on the UK Medical Eligibility Criteria (UKMEC), which categorizes potential contraindications and cautions on a four-point scale. UKMEC 1 indicates no restrictions for use, while UKMEC 2 suggests that the benefits outweigh the risks. UKMEC 3 indicates that the disadvantages may outweigh the advantages, and UKMEC 4 represents an unacceptable health risk. Examples of UKMEC 3 conditions include controlled hypertension, a family history of thromboembolic disease in first-degree relatives under 45 years old, and current gallbladder disease. Examples of UKMEC 4 conditions include a history of thromboembolic disease or thrombogenic mutation, breast cancer, and uncontrolled hypertension. Diabetes mellitus diagnosed over 20 years ago is classified as UKMEC 3 or 4 depending on severity. In 2016, breast feeding between 6 weeks and 6 months postpartum was changed from UKMEC 3 to UKMEC 2.

Sickle cell anaemia is a genetic disorder that follows an autosomal recessive pattern of inheritance. This means that an individual must inherit two copies of the mutated gene, one from each parent who are carriers of the condition. Huntington’s Disease is an example of an autosomal dominant condition, while Fragile X syndrome is an example of an X-linked dominant condition. Haemophilia is an example of an X-linked recessive condition, and alpha-1 antitrypsin deficiency is an example of a co-dominant condition.

Sickle-cell anaemia is a genetic disorder that occurs when abnormal haemoglobin, known as HbS, is produced due to an autosomal recessive condition. This condition is more common in individuals of African descent, as the heterozygous condition provides some protection against malaria. About 10% of UK Afro-Caribbean’s are carriers of HbS, and they only experience symptoms if they are severely hypoxic. Homozygotes tend to develop symptoms between 4-6 months when the abnormal HbSS molecules replace fetal haemoglobin.

The pathophysiology of sickle-cell anaemia involves the substitution of the polar amino acid glutamate with the non-polar valine in each of the two beta chains (codon 6) of haemoglobin. This substitution decreases the water solubility of deoxy-Hb, causing HbS molecules to polymerise and sickle RBCs in the deoxygenated state. HbAS patients sickle at p02 2.5 – 4 kPa, while HbSS patients sickle at p02 5 – 6 kPa. Sickle cells are fragile and haemolyse, blocking small blood vessels and causing infarction.

The definitive diagnosis of sickle-cell anaemia is through haemoglobin electrophoresis.

Pre-eclampsia can be diagnosed based on the presence of high levels of protein in the urine and hypertension. To prevent the development of eclampsia, magnesium sulphate is administered, while labetalol is used to manage high blood pressure. If a cardiotocography (CTG) shows late decelerations and foetal bradycardia, this is a concerning sign and may necessitate an emergency caesarean section. Induction would not be recommended if the CTG is abnormal.

Cardiotocography (CTG) is a medical procedure that measures pressure changes in the uterus using either internal or external pressure transducers. It is used to monitor the fetal heart rate, which normally ranges between 100-160 beats per minute. There are several features that can be observed during a CTG, including baseline bradycardia (heart rate below 100 beats per minute), which can be caused by increased fetal vagal tone or maternal beta-blocker use. Baseline tachycardia (heart rate above 160 beats per minute) can be caused by maternal pyrexia, chorioamnionitis, hypoxia, or prematurity. Loss of baseline variability (less than 5 beats per minute) can be caused by prematurity or hypoxia. Early deceleration, which is a decrease in heart rate that starts with the onset of a contraction and returns to normal after the contraction, is usually harmless and indicates head compression. Late deceleration, on the other hand, is a decrease in heart rate that lags behind the onset of a contraction and does not return to normal until after 30 seconds following the end of the contraction. This can indicate fetal distress, such as asphyxia or placental insufficiency. Variable decelerations, which are independent of contractions, may indicate cord compression.

The Addenbrookes Cognitive Exam (ACE-3) is a reliable tool for detecting dementia, with a score of 82 or less indicating a strong likelihood of dementia. The exam assesses five domains: Memory, Attention, Fluency, Language, and Visuospatial. Alzheimer’s dementia typically results in a global deficit across all domains, with later deficits in memory and attention due to damage in the medial temporal lobe. Frontotemporal dementia primarily affects fluency and language due to damage in the frontal lobe. Vascular dementia deficits vary depending on the location and severity of previous strokes, and there is no consistent pattern seen in ACE-3 examinations. Mild cognitive impairment (MCI) is a precursor to many forms of dementia, with an ACE-3 score of 82-88 indicating MCI. In this scenario, the patient’s score of 68 rules out MCI as a diagnosis.

Alzheimer’s disease is a type of dementia that gradually worsens over time and is the most common form of dementia in the UK. The risk factors for Alzheimer’s disease include increasing age, family history of the disease, and certain genetic mutations. Inherited forms of the disease are caused by mutations in the amyloid precursor protein, presenilin 1, and presenilin 2 genes. Additionally, the apoprotein E allele E4 and Caucasian ethnicity are also risk factors for Alzheimer’s disease.

The pathological changes associated with Alzheimer’s disease include widespread cerebral atrophy, particularly in the cortex and hippocampus. Microscopically, cortical plaques and intraneuronal neurofibrillary tangles are present due to the deposition of type A-Beta-amyloid protein and abnormal aggregation of the tau protein. The hyperphosphorylation of the tau protein has been linked to Alzheimer’s disease. Furthermore, there is a deficit of acetylcholine due to damage to an ascending forebrain projection.

Neurofibrillary tangles are partly made from a protein called tau, which interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules. In Alzheimer’s disease, tau proteins are excessively phosphorylated, impairing their function.

Angina pectoris is a condition that can be managed through various methods, including lifestyle changes, medication, percutaneous coronary intervention, and surgery. In 2011, NICE released guidelines for the management of stable angina. Medication is an important aspect of treatment, and all patients should receive aspirin and a statin unless there are contraindications. Sublingual glyceryl trinitrate can be used to abort angina attacks. The first-line medication should be either a beta-blocker or a calcium channel blocker, depending on the patient’s comorbidities, contraindications, and preferences. If a calcium channel blocker is used as monotherapy, a rate-limiting one such as verapamil or diltiazem should be used. If used in combination with a beta-blocker, a longer-acting dihydropyridine calcium channel blocker should be used. Beta-blockers should not be prescribed concurrently with verapamil due to the risk of complete heart block. If the initial treatment is not effective, medication should be increased to the maximum tolerated dose. If a patient is still symptomatic after monotherapy with a beta-blocker, a calcium channel blocker can be added, and vice versa. If a patient cannot tolerate the addition of a calcium channel blocker or a beta-blocker, other drugs such as long-acting nitrates, ivabradine, nicorandil, or ranolazine can be considered. Nitrate tolerance is a common issue, and patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimize the development of nitrate tolerance. This effect is not seen in patients who take once-daily modified-release isosorbide mononitrate. If a patient is taking both a beta-blocker and a calcium-channel blocker, a third drug should only be added while awaiting assessment for PCI or CABG.

Oligohydramnios is a condition that occurs during pregnancy when there is a shortage of amniotic fluid. This can result in a smaller symphysiofundal height.

Oligohydramnios is a condition characterized by a decrease in the amount of amniotic fluid present in the womb. The definition of oligohydramnios varies, but it is generally considered to be present when there is less than 500ml of amniotic fluid at 32-36 weeks of gestation or an amniotic fluid index (AFI) that falls below the 5th percentile.

There are several potential causes of oligohydramnios, including premature rupture of membranes, Potter sequence, bilateral renal agenesis with pulmonary hypoplasia, intrauterine growth restriction, post-term gestation, and pre-eclampsia. These conditions can all contribute to a reduction in the amount of amniotic fluid present in the womb, which can have significant implications for fetal development and health. It is important for healthcare providers to monitor amniotic fluid levels and identify any potential causes of oligohydramnios in order to provide appropriate care and support for both the mother and the developing fetus.

When there is suspicion of a spinal epidural abscess, a complete MRI of the spine is necessary to detect any skip lesions.

To accurately diagnose a spinal epidural abscess, a full spine MRI is essential. Neither plain x-rays nor CT scans can effectively identify the abscess. It is necessary to scan the entire spine, not just the suspected area, as there may be multiple separate abscesses that are not connected. The MRI should be requested and performed as soon as possible.

Understanding Spinal Epidural Abscess

A spinal epidural abscess (SEA) is a serious condition that occurs when pus collects in the spinal epidural space, which is the area surrounding the spinal cord. This condition requires immediate medical attention to prevent further damage to the spinal cord. SEA can be caused by bacteria that enters the spinal epidural space through contiguous spread from adjacent structures, haematogenous spread from concomitant infection, or direct infection. Patients with immunosuppression are at a higher risk of developing SEA. The most common causative micro-organism is Staphylococcus aureus. Symptoms of SEA include fever, back pain, and focal neurological deficits according to the segment of the cord affected.

To diagnose SEA, doctors may perform blood tests, blood cultures, and an infection screen. An MRI of the whole spine is necessary to identify the extent of the abscess. If the primary source of infection is not clear, further investigations may be required, such as echocardiography and dental x-rays. Treatment for SEA involves a long-term course of antibiotics, which may be refined based on culture results. Patients with large or compressive abscesses, significant or progressive neurological deficits, or those who are not responding to antibiotics alone may require surgical evacuation of the abscess.